We will investigate two fundamental processes of genetic control in E. coli, which are models for genetic regulation in all cells. 1. The protein encoded by bacteriophage lambda gene Q invokes phage late gene expression by acting in a specific operon as a transcription antiterminator. Antitermination is an important mechanism of regulation in bacteria, and possibly in all cells and viruses. We will determine how lambda Q protein is engaged by RNA polymerase at a genome-specific site near the promoter, using chemical and nuclease protection methods to probe its interaction with DNA, and using mutations we will make that change this interaction in specific ways. We will determine how Q protein modifies the properties of RNA polymerase to allow it to pass transcription terminators, and how it changes the ability of RNA polymerase to pause at characteristic sites. We will investigate the role of the transcription factor NusA protein in antitermination. 2. In addition to catalyzing DNA strand exchange in genetic recombination, the E. coli RecA protein mediates induction of the SOS genes, which include DNA repair functions required for mutagenesis by most important carcinogens. Carcinogens are also inducers of SOS genes (and phage lambda), because they lead to activation of RecA protein to bind and destroy by proteolytic cleavage the LexA repressor of the SOS genes, as well as temperate phage repressors. To test the model that induction occurs when chromosome replication uncovers gaps in DNA at the sites of carcinogen-induced lesions, we will determine the relation between LexA cleavage and DNA replication. To test the universality of this regulation, we will study an analogue of RecA protein in the distantly related bacterium B. subtilis.